Amiodarone-induced thyrotoxicosis type 1 during the treatment of cardiovascular diseases: features of a clinical case

Background. Treatment of patients with comorbid pathology, including hypertension, coronary heart disease with atrial fibrillation, often requires the use of amiodarone. Unfortunately, the latter in some cases is accompanied by complications, inclu­ding thyroid dysfunction. The most serious situation develops when amiodarone-induced thyrotoxicosis occurs, which leads to an additional toxic effect on the myocardium and changes in the sensitivity of the cardiovascular system to catecholamines. The manifestation of amiodarone-induced thyrotoxicosis is not always typical, which causes certain difficulties in diagnosis and treatment, especially in geriatric patients with comorbid conditions. The purpose of the study: to analyze a clinical case of amiodarone-induced thyrotoxi­cosis type 1 in an elderly patient suffering from hypertension and coronary heart disease with a previous myocardial infarction, heart rhythm disorders; to find out the peculiarities of clinical manifestations of thyroid dysfunction, approaches to diagnosis and treatment. Materials and methods. A clinical case of treatment of a patient with cardiovascular pathology complicated by the development of thyroid dysfunction when using amiodarone is considered: the data of medical history, objective examination, results of laboratory and instrumental research and treatment outcomes are presented and analyzed. Results. Patient P. aged 88 years old was hospitali­zed to the cardiology department with clinical signs of thyrotoxic cardiomyopathy, encephalopathy, myopathy, dermopathy. He has been sick for about 45 years, has a history of myocardial infarction; received antihypertensive drugs, statins, nitrates, and antithrombotic drugs on a permanent basis. Given the severity of the condition and the occurrence of atrial fibrillation, amiodarone 200 mg daily was prescribed a year ago. Examination of the patient revealed a signi­ficant weight loss, signs of heart failure stage IIA with a decrease in ejection fraction to 34–36 %, combined rhythm disturbances, in particular atrial fibrillation. According to the laboratory and instrumental examination, there was a sharp decrease in thyroid-stimulating hormone to 0.007 μIU/ml with a moderate increase in free T4 and almost normal size of the thyroid gland, moderately increased echogenicity with areas of hypervascularization and a small heterogeneous node in the right lobe. In addition, an increase in erythrocyte sedimentation rate, mild anemia, and slight hypercreatininemia were observed. Taking into account the comorbid pathology, the age of the patient, changes in the thyroid gland simultaneously with thyroid dysfunction, progression of heart failure and heart rhythm disturbances against the background of long-term amiodarone administration, a diagnosis of amiodarone-induced thyrotoxicosis type 1 was made. First of all, amiodarone was discontinued, thiama­zole 20 mg daily was prescribed, as well as anti-anemic and sedative drugs. Potassium perchlorate was not used. After four months, it was possible to achieve an euthyroid state without adverse reactions from thyrostatic therapy. No recurrence of thyrotoxicosis was observed during the year. Conclusions. Considering that the use of amiodarone in comorbid elderly patients, including those with predominant cardiovascular manifestations, may be accompanied by damage to the thyroid gland, it is necessary to carefully monitor the state and function of the gland, both before prescribing the drug and during therapy to avoid possible development of amiodarone-induced conditions, especially thyrotoxicosis. Treatment of amiodarone-induced thyrotoxicosis type 1 must include thyrostatic therapy, with the do­sage adjusted based on the patient’s age, comorbid conditions. The duration should be determined by the achievement of euthyroidism with further medical support.